Semapimod: Difference between revisions

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Semapimod, formerly known as CNI-1493, was first developed to inhibit nitric oxide synthesis by inflammatory macrophages, via inhibition of the uptake of arginine which macrophages require for nitric oxide synthesis.<ref>{{cite pmid|8529104}}</ref> Subsequently it was found that suppression of nitric oxide synthesis occurred even at semapimod concentrations 10-fold less than required for inhibition of arginine uptake, suggesting that this molecule was a more general inhibitor of inflammatory responses.<ref>{{cite pmid|8642296}}</ref>
Semapimod, formerly known as CNI-1493, was first developed to inhibit [[nitric oxide]] synthesis by inflammatory [[macrophages]], via inhibition of the uptake of [[arginine]] which macrophages require for nitric oxide synthesis.<ref>{{cite pmid|8529104}}</ref> Subsequently it was found that suppression of nitric oxide synthesis occurred even at semapimod concentrations 10-fold less than required for inhibition of arginine uptake, suggesting that this molecule was a more general inhibitor of [[inflammatory]] responses.<ref>{{cite pmid|8642296}}</ref> Further work revealed that semapimod suppressed the [[translation (genetics)|translation]] efficiency of [[tumor necrosis factor]] production.<ref>{{cite pmid|8632999}}</ref> Specifically, semapimod was found to be an inhibitor of [[p38 kinase|p38 MAP kinase]] activation.<ref>{{cite pmid|9205949}}</ref>


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Revision as of 17:02, 9 May 2009

Semapimod
Identifiers
  • N,N'-bis[3,5-bis[N-(diaminomethylideneamino)-C-methylcarbonimidoyl]phenyl] decanediamide tetrahydrochloride
CAS Number
Chemical and physical data
FormulaC34H56Cl4N18O2
Molar mass890.73984 g/mol g·mol−1
3D model (JSmol)
  • CC(=NN=C(N)N)C1=CC(=CC(=C1)NC(=O)CCCCCCCCC(=O)NC2=CC(=CC(=C2)C(=NN=C(N)N)C)C(=NN=C(N)N)C)C(=NN=C(N)N)C.Cl.Cl.Cl.Cl

Semapimod, formerly known as CNI-1493, was first developed to inhibit nitric oxide synthesis by inflammatory macrophages, via inhibition of the uptake of arginine which macrophages require for nitric oxide synthesis.[1] Subsequently it was found that suppression of nitric oxide synthesis occurred even at semapimod concentrations 10-fold less than required for inhibition of arginine uptake, suggesting that this molecule was a more general inhibitor of inflammatory responses.[2] Further work revealed that semapimod suppressed the translation efficiency of tumor necrosis factor production.[3] Specifically, semapimod was found to be an inhibitor of p38 MAP kinase activation.[4]

  1. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 8529104, please use {{cite journal}} with |pmid=8529104 instead.
  2. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 8642296, please use {{cite journal}} with |pmid=8642296 instead.
  3. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 8632999, please use {{cite journal}} with |pmid=8632999 instead.
  4. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 9205949, please use {{cite journal}} with |pmid=9205949 instead.